Good afternoon, Professor and all senior collegues

Thank you for the give time and opportunity, today I would
like to give a presentation my TBR about Guillain Barre
Syndrom

When patien come to you and complain for the weakness he

feel, asenderen paralysis and sensory disturbance. So what
kind of differential diagnosis that must be think of ?

So we must have a deep analysis of physical examination. We

can find areflexic motor paralysis with or without sensory
disturbance

To firm GBS, we must understand what is GBS definition…

Learn about GBS is important, because the incidence of GBS

is quite high… EPIDEMIOLOGY

Anatomy and physiology

Nerve dysfungtion in GBS is cause by an immune attack on the

nerve cells of the peripheral nervous system and their support
structures.

The nerve cells have their body in the spinal cord and a long
projection that carries electrical nerve impulses to the
neuromuscular junction, where the impulse is transferred to
the muscle
Axons are wrapped in a sheath of Schwann cells that contain
myelin. Beetween Schwann cells are gaps, we called it nodes of
ranvier, where the axon is exposed

Patophysiology

Different type of GBS feature different types of immune

attack. The demyelinating variant features damage to the
myelin sheats by white blood cell. This process is preceded by
activation of group of blood protein known as complement.

Target invasion of immune system is ganglioside, Gangliosida

role in the interaction between cells, modulation of the
receptor , and growth regulation
widely distributed in the nervous tissue , especially in the
nodes of Ranvier
So if Nodus of Ranvier damage, the impulse from reseptor to
the efector will be late.
Subtye of GBS

We know there are few subtye of GBS variant, in here there

is variant of GBS there is…

Investigations

The first symptoms of GBS are numbness and tingling,

weakness and pain, alone or in combination. This is followed by
weakness of legs and arms that is symmetrical and as time
goes the condition worsens. On the neurogical examination,
characteristic feature are the reduced power and reduced or
absent tendo reflex

Lumbal pungtion

Electromyography

Electromyography and nerve condution studies may show

prolonged distal latencies, conduction slowing, condution block
and temporal dispersion of compound muscle action potentioal
in demyelinating cases.

F wave and H reflex may be prolonged or absent. Needle EMG

is frequently normal in acute cases. Reduced, neuropathy
recruitment in weak muscle can be seen. Fibrillation can be
seen on needle EMG if some axon injury occurs after 3 to 4
week. In primary axonal damage, the findings include reduced
amplitude of the action potential without condution slowing

Clinical Phase

there are 4 phases of GBS, which we can see by the time

1. Latency phase : The time between infection arises /
prodromal that preceded it until the onset of clinical
symptoms
2. Progresif phase : paralysis began increasing until the
maximum weight
3. Plateau phase : Paralysis has been maximized and
settled
 4. Recovery phase : Repair phase motor paralysis for
months

Closing
I would like to thank for Prof wid for the advice and guidance.
And I would to thanks for all senior colleagus for thr
willingness to attend this presentation
Thank you and good day